Scientists at the University of Virginia School of Medicine have discovered a cluster of brain cells that control the body’s response to acute anemia, which could benefit efforts to develop new treatments for traumatic injuries.
The search shows a collection of neurons that respond by maintaining blood pressure while the blood is low. However, severe anemia eventually leads to cardiac and vascular constriction – a condition characterized by sudden and dangerous loss of blood – a condition called “disintegration bleeding” – and new results shed light on why this happens.
“As blood is reduced, the brain coordinates the cardiovascular response, which supports blood flow to critical organs such as the heart and brain,” said George Souza, a PhD researcher at UVA’s Department of Pharmacology. “Our study shows that the cardiovascular response to anemia depends on changes in the activity of a few hundred neurons in the brain.”
Under pressure
New findings from Stephen Abbott, PhD, and colleagues at UVA shed light on the important processes that the body uses to maintain blood pressure. Neurons described by Abbott and his team – aptly known as “adrenergic C1 neurons” – monitor blood pressure and act when blood is low. When neurons are depleted of blood, they increase the activity of nerves which causes the blood vessels to constrict and maintain proper blood pressure.
Scientists were able to determine this using advanced imaging and a technique called optogenetics that allowed light to be remotely controlled by neurons. Their research showed that C1 neurons become overactive when blood is depleted and thus blood pressure is maintained. But these neurons become inactive due to severe blood loss, resulting in cardiovascular damage.
Dissociative bleeding is a precursor to hemorrhagic shock, in which the body begins to shut down. But scientists found that reactivating C1 neurons in laboratory rats restored both blood pressure and heart rate.
“Our study suggests that reactivating the brain pathways that control blood pressure during dissected bleeding effectively reverses cardiovascular damage. We think this suggests that neuromodulation of the pathways described by our study may be a beneficial adjuvant treatment for low blood pressure after anemia, “said Abbott of UVA’s Department of Pharmacology.
Scientists note that a number of factors may have contributed to the decrease in the activity of C1 neurons during the onset of degenerative bleeding. More research is needed on that front. But the team’s findings identify important new directions for future research.
“These findings illustrate the importance of brain-body interactions when there is a decrease in blood flow and provide a new perspective on the root cause of cardiovascular contraction,” Abbott said.
Published anemia findings
The researchers published their findings in the scientific journal Cell Reports. The research team includes George M.P.R. Souza, Ruth L. Storneta, Daniel S. Storneta, Patrice g. Guyanet and Stephen B.G. Abbott. All are part of UVA’s pharmacology department.
The work is funded by the American Heart Association, grant 19POST34430205, and the National Institutes of Health, HL148004, HL28785 and HL074011.